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PubMed2006

Spatial and temporal relationship between monocyte chemoattractant protein-1 expression and spinal glial activation following peripheral nerve injury.

Peripheral nerve injury can induce spinal microglial/astrocyte activation. Substances released by activated glial cells excite spinal nociceptive neurons. Pharmacological disruption of glial activation or antagonism of substances released by activated glia prevent or reverse pain hypersensitivity. It is not known, however, what causes spinal cord glia to shift from a resting to an activated state. In an attempt to understand the potential role of monocyte chemoattractant protein-1 (MCP-1) in triggering spinal glial activation and its contribution to the development of neuropathic pain, we investigated the effect of peripheral nerve injury on MCP-1 expression in dorsal root ganglia (DRG) and the spinal cord, and established its temporal relationship with activation of spinal microglia and astrocytes. We observed that MCP-1 was induced by chronic constriction of the sciatic nerve in DRG sensory neurons, spinal cord motor neurons and in the superficial dorsal horn, ipsilateral to the injury. Neuronal MCP-1 induction was followed by surrounding microglial activation. After peaking at day 7 after injury, MCP-1 levels began to decline rapidly and had returned to baseline by day 150. In contrast, microglial activation peaked by day 14 and declined afterwards to reach a lower, yet significantly raised level beyond day 22 and remained increased until the end of the test period. Astrocyte activation became detectable later, progressed more slowly and also remained increased until the end of the test period, in parallel with a decreased nociceptive threshold. Our results suggest that neuronal MCP-1 may serve as a trigger for spinal microglial activation, which participates in the initiation of neuropathic pain. Delayed, sustained astrocyte activation may participate with microglia in the persistent phase of pain hypersensitivity.

Activating Transcription Factor 3↗
PubMed2000

The relationship between melanocytes and peripheral nerve sheath cells (Part I): melanocytic nevus (excluding so-called "blue nevus") with peripheral nerve sheath differentiation.

Among thousands of specimens of melanocytic nevi, not including giant congenital melanocytic nevus or blue nevus, 42 melanocytic nevi that showed peripheral nerve sheath differentiation were collected. The patterns of melanocytic nevi with peripheral nerve sheath differentiation may be classified into three groups: 1) "neurotized and neural nevi" with nests of "neuroid cords" and "nevic corpuscles" (the most common pattern); 2) nerve fascicle-like structures with no relation to neurotized and neural nevi; and 3) palisading melanocytes of a nevus in nests of conventional melanocytic nevi (a rare pattern). Each pattern may represent a different expression of nerve sheath differentiation in melanocytic nevi. Some melanocytic nevi with nerve fascicle-like structures show discrete structures closely resembling authentic nerve fascicles, confirming a close relationship between melanocytes and peripheral nerve sheath cells (Schwann cells and probably perineurial cells in part) and suggesting derivation of the two types of cells from common precursor cells of the neural crest and their de novo development in the dermis rather than by Abtropfung of melanocytes from the epidermis. In addition, the high prevalence of Unna, Miescher, and superficial congenital nevi in melanocytic nevi with peripheral nerve sheath differentiation suggests a different character or process for these congenital melanocytic nevi than for Clark and Spitz nevi (junctional and compound types).

Cell Differentiation↗
PubMed1998

[The protective effects of nerve growth factor on peripheral nerve injury].

The protective effects of nerve growth factor (NGF) on peripheral nerve injury and sensory neuron growth were studied in three models: peripheral sympathetic nerve injury induced by intraperitoneal injection of 6-hydrodopamine (6-OHDA), mechanically injured ulnar nerve and cultured dorsal root ganglion (DRG) of newborn rats in vitro. The results indicate that NGF dose-dependently increased norepinephrine content in mouse submandibular gland and cell numbers of C7 (seventh cervical vertebra), T1 (first thoracic vertebra) dorsal root ganglion in rabbits, and also dramatically promoted the growth of neuronal projections in cultured DRG. These results suggest that NGF has significant neuroprotective action in peripheral nerve injury and a strong neuronutrition on sensory neuron.

Animals↗
PubMedDate not supplied

Use of a newly developed artificial nerve conduit to assist peripheral nerve regeneration across a long gap in dogs.

There is now considerable evidence that peripheral nerves have the potential to regenerate if an appropriate microenvironment is provided. However, there are only a few reports of the successful use of artificial nerve conduits to repair major nerve defects more than 30 mm in length. In this study, we examined nerve regeneration across a long gap in the dog peroneal nerve using a novel artificial nerve conduit developed by our group. The conduit consists of a polyglycolic acid (PGA) collagen tube filled with laminin coated collagen fibers. In 12 dogs, the nerve conduit was implanted across an 80 mm gap in the left peroneal nerve. Three months after surgery, compound muscle action potentials (CMAPs) and somatosensory evoked potentials (SEPs) were detected. Evaluation of locomotor function revealed obvious limping for up to 3 months, but no marked difficulty in walking by 6 months. Microscopic observation of the regenerated nerve segment at 12 months showed numerous myelinated nerve fibers, which were smaller in diameter and enclosed in a thinner myelin sheath than normal axons. These results suggest that our artificial nerve conduit has potential usefulness in enhancing peripheral nerve regeneration, even across large gaps.

Action Potentials↗
PubMed2005

Stimulation of neurite outgrowth in a human nerve scaffold designed for peripheral nerve reconstruction.

The clinical outcome of microsurgical reconstruction of large peripheral nerve lesions depends on the availability of suitable graft material. Allogenic nerve grafts are rejected by the immune system. Extracellular-matrix proteins, in contrast to the resident cells, are of low immunogenicity in allografts. Here, human tibial nerve segments were extracted with lysophosphatidyl choline. The obtained cell-free and myelin-free scaffold consisted of empty endoneural tubes with maintained extracellular matrix architecture. The nerve scaffold had mechanical properties comparable to intact nerve, making it suitable for microsurgical reconstruction. Sections of the nerve scaffold were tested as a substrate for the adhesion and neuronal differentiation of human neuroblastoma-derived LAN-5 cells. Nerve extraction removed laminin-2, an isoform of laminin important for peripheral nerve regeneration. Laminin-2 reloading of the nerve scaffold did not improve cell adhesion and axon growth. Chemical crosslinking of heparan sulfate, on the other hand, increased the percentage of adherent cells with outgrowing neurites from 48 to 85%. Combined laminin-2 reloading and heparan sulfate crosslinking reduced the percentage of neurite-forming cells to 22% of the number of adherent cells. Implantation of the nerve scaffold into the peritoneal cavity of mice was not cytotoxic, and neovascularization of the graft material was observed within weeks. In conclusion, extraction of human nerve with detergents revealed a biocompatible nerve scaffold supporting neuronal cell adhesion. Heparan sulfate crosslinking to the scaffold surface improved neurite outgrowth, presumably mediated by midkine, a member of the neurokine family of growth factors, which is secreted by neuroblastoma-derived cells and binds to heparan sulfate.

Animals↗
PubMed1990

Ultrastructural changes in glial cells during regeneration of cockroach peripheral nerve.

After peripheral nerve 5 in the cockroach Periplaneta americana was cut, changes occurring in the glial cells in the proximal stump were studied immediately after damage and during the process of nerve regeneration. During the first week haemocytes accumulated outside the nerve and morphologically similar granule-containing cells appeared inside the nerve. These cells were involved in phagocytic activity. Between the second and the fourth week, signs of regeneration were distinguishable; many small axonal sprouts were formed which were surrounded by glial processes, and the nerve stump increased in length. During this period the glial cells produced large amounts of extracellular material in which the bundles of axons and glia were embedded. The structural differences between glial and perineurial cells were lost during these stages of regeneration and there was no restriction to the penetration of the extracellular tracer lanthanum. After 8 weeks, reinnervation of the muscles had taken place, perineurial and glial cells were again distinguishable, and the perineurial cells were able to exclude lanthanum.

Animals↗
PubMed1990

Peripheral nerve pathways to neurons in the guinea pig inferior mesenteric ganglion determined electrophysiologically after chronic nerve section.

Peripheral synaptic pathways to neurons in the guinea pig inferior mesenteric ganglion (IMG) were studied. Nerve trunks innervating neurons in the ganglion were surgically sectioned and intracellular electrical responses to nerve stimulation were measured 6-8 days after surgery. In all animals ganglia were decentralized by removal of the lumbar sympathetic chain ganglia L2 through L4 and in addition two peripheral nerves were sectioned leaving the ganglion innervated by only one peripheral nerve. Fast and slow excitatory postsynaptic potential (EPSP) were evoked with electrical stimulation of each of the nerve trunks and with distension of the colon. The thresholds to evoke fast EPSPs and the amplitude of slow EPSPs were compared for each nerve trunk among the different surgical groups including sham-operated controls and completely denervated ganglia. Both fast and slow EPSPs could be evoked electrically from each intact peripheral nerve trunk after the other three nerve trunks had been sectioned, which demonstrates that nerve fibers with cell bodies in the regions innervated by the peripheral nerves make functional synaptic connections with neurons in the inferior mesenteric ganglion. In general, nerve sections increased the threshold for evoking fast EPSPs and decreased the amplitude of electrically-evoked slow EPSPs compared to control ganglia. Synaptic potentials could also be evoked with stimulation of cut nerve trunks, demonstrating that branches of nerve fibers from peripheral nerves enter other nerve trunks. The hypogastric nerve was unique in that branches of axons eliciting fast but not slow synaptic potentials in the ganglion entered this nerve trunk. Distension-induced fast and slow EPSPs were present only if the lumbar colonic nerve was intact and they were not altered by section of the other nerve trunks. In contrast, the slow EPSPs evoked with electrical stimulation of the lumbar colonic nerve were significantly smaller when at least one other nerve trunk was sectioned suggesting that the axon branches from other nerve trunks which enter the lumbar colonic nerve are not activated by distension. These studies demonstrate that neurons eliciting either fast or slow synaptic potentials with cell bodies in regions innervated by the peripheral nerve trunks make functional synaptic connections with neurons of the inferior mesenteric ganglion. The results also suggest that the majority of mechanosensory neurons mediating excitatory synaptic responses to colon distension are neurons with a peripheral cell body.

Action Potentials↗
PubMed1996

Fatty acid binding protein is induced in neurons of the dorsal root ganglia after peripheral nerve injury.

Peripheral nerve trauma induces the expression of genes presumed to be involved in the process of nerve degeneration and repair. In the present study, an in vivo paradigm was employed to identify molecules which may have important roles in these processes. A cDNA library was constructed with RNA extracted from rat dorsal root ganglia (DRG) 3 days after a sciatic nerve crush. After differential hybridization to this library, several cDNAs were identified that encoded mRNAs that were upregulated in the DRG ipsilateral to the crush injury, as opposed to the contralateral or naive DRG. Approximately 0.15% of all the clones screened were found to be induced. This report presents the types of induced sequences identified and characterizes one of them, DA11. The 0.7 kb DA11 full length cDNA clone contains a 405 nucleotide open reading frame that encodes a putative protein of 15.2 kDa (135 amino acid residues) and is a member of the family of fatty acid binding proteins (FABP). The DA11 protein differs by one amino acid residue from the sequence of the C-FAPB protein and by eight residues from the sequence of mal1, proteins found in rat and mouse skin, respectively. Northern and Western blot analyses showed that the DA11 mRNA and protein were induced in the injured DRG. Furthermore, studies using antibodies generated against DA11 found that the DA11-like immunoreactivity was more pronounced in the nuclei of neurons located in the DRG ipsilateral to the sciatic cut than those located in the contralateral DRG. The induction of DA11 mRNA and protein in DRG neurons suggests, for the first time, the involvement of a neuronal FABP in the process of degeneration and repair in the nervous system.

Amino Acid Sequence↗
PubMed1982

Tropism in nerve regeneration in vivo. Attraction of regenerating axons by diffusible factors derived from cells in distal nerve stumps of transected peripheral nerves.

We re-examined the hypothesis of Cajal3, later refuted by Weiss and Taylor20, that cells in distal stumps of transected peripheral nerves exert an attractive (tropic) effect on regenerating axons. This question was re-assessed in vivo using surgical materials and assay procedures not available to those workers. Proximal stumps of transected rat sciatic or cat peroneal nerves were inserted into the single inlet end of a hollow, Y-shaped Silastic implant. Regenerating axons were provided with alternative targets consisting of a vacant arm vs one occupied by a sciatic nerve graft (rat), or a tibial (Tout) vs peroneal (Pout) distal nerve stump (cat). In some cases Pout was rendered metabolically compromised relative to Tout by exposing the former to dry ice and inhibitors of DNA and RNA synthesis. At 4.5 or 6 weeks postoperatively, the number of regenerating axons in each fork of the implant was assessed by morphometric analysis (total number of non-myelinated and myelinated axons greater than 1 micron in diameter at 4.5 weeks, and total number of myelinated axons at 6 weeks postoperatively), or by quantification of an axonally transported label. Rat sciatic nerve fibers exclusively regenerated toward the nerve graft, suggesting the existence of a neurotropic lure. In cats, morphometric analysis revealed a 10-(4.5 week) and 6-fold (6 week) greater number of axons growing towards untreated Tout vs treated Pout. When both distal stumps were untreated, more axons were seen in forks leading to Pout. Analysis of transported label confirmed the preferential growth of axons towards untreated Tout vs treated Pout for both motor and sensory axons. In separate experiments, Nuclepore filters (0.2 microns, pore size) were inserted between distal nerve stumps and outlet ends of Silastic implants. Preferential regeneration toward untreated stumps was observed if the distance between proximal and distal nerve stumps was equal to but not greater than 4-5 mm. These results suggest that peripheral nerve fiber regeneration in vivo can be directed by cells in distal stumps of transected nerves, and that this effect can be mediated over distances of several millimeters via diffusible factors.

Animals↗
PubMed2004

Worsening myelopathy masked by peripheral nerve disorders.

BACKGROUND/OBJECTIVE: Peripheral nerve disorders--whether due to peripheral nerve entrapment or to polyneuropathy--can alter the signs of myelopathy, masking both the sensory loss and distal hyperreflexia. Diagnosis of worsening myelopathy may be missed when there is a coexisting peripheral nerve disorder. METHODS: This study is a case description and analysis of 3 consecutive cases identified over 2 years. RESULTS: Three cases were identified in which the diagnosis of worsening myelopathy was missed and treatment was delayed because neurologic decline was attributed to a coexisting peripheral nerve disorder. This report describes 2 cases of posttraumatic syringomyelia masked by superimposed peripheral nerve entrapments and 1 case of cervical myelopathy due to cervical spinal stenosis from ossification of the posterior longitudinal ligament masked by diabetic polyneuropathy. CONCLUSION: It is important to continually question whether the working diagnosis of peripheral nerve disorder explains the clinical findings, given neurologic decline; or whether a superimposed worsening myelopathy may coexist. Early diagnosis of worsening myelopathy is important, because prompt treatment of syringomyelia and myelopathy due to cervical spinal stenosis may yield better outcomes. Early diagnosis is aided by (a) considering alternative and multiple diagnoses, (b) assessing spinothalamic as well as posterior column sensation and assessing these sensory modalities for proximal as well as distal limbs, (c) assessing tendon hyperreflexia of proximal as well as distal limb muscles, and (d) utilizing electrodiagnostic tests that can identify myelopathy.

Adult↗
PubMedDate not supplied

An ultrastructural study of blood vessels in peripheral nerves of leprosy patients: blood vessels in peripheral nerves.

Ultrathin sections of nerves of tuberculoid and lepromatous leprosy were examined in an electron microscope for changes in endoneural blood vessels. In the tuberculoid nerves, hypertrophy of endothelial cells was the most prominent feature. This was to such an extent that the lumen of blood vessel was often closed. Endoneural blood vessels showed multilayers separated by collagen and ground substances. In contrast, in the lepromatous nerves, there was no hypertrophy of endothelial cells in the blood vessels and the lumen of the vessels was open. M. leprae were seen within the endothelial cells and these organisms were intact and probably viable. These observations suggest a possible involvement of endoneural blood vessels which may contribute to nerve damage in leprosy.

Endothelium, Vascular↗
PubMed1999

Nerve growth factor enhances peripheral nerve regeneration in non-human primates.

Fibronectin mat implants impregnated with NGF have been successfully used in rat nerve regeneration model. The aim of this study was to assess their action in a primate model. Mats were implanted into a 5 mm gap in a peripheral nerve in Macaca fascicularis monkeys, either alone (Fn) or in the presence of nerve growth factor (Fn + NGF). Four months postoperatively, the regenerated nerve was analysed by light microscopy, and target skin reinnervation was assessed by quantification of cutaneous nerve terminals immunostained with protein gene product (PGP) antibodies. The diameter of the regenerated nerve was similar in Fn + NGF grafts and nerve autografts, but significantly larger for plain Fn grafts with evidence of more connective tissue surrounding the axons. Myelinated fibres counts showed similarities in normal control nerve, nerve autograft and Fn + NGF graft groups. However, in nerve grafted with plain Fn mats the regenerating fibres were lower in number and showed a wider variability in diameter and myelination, resulting in a significantly smaller G-ratio (axonal diameter/myelinated fibre diameter). The amount of cutaneous reinnervation was lowest in Fn graft group, while comparable amounts of skin reinnervation were observed in the Fn + NGF and autograft groups. These results suggest that Fn-mats are a suitable conduit to promote peripheral nerve regeneration also in primate, and supplying NGF locally at the lesion site can further enhance nerve regrowth.

Animals↗
PubMed1999

Role of thyroid hormones and their receptors in peripheral nerve regeneration.

After peripheral nerve injury in adult mammals, reestablishment of functional connections depends on several parameters including neurotrophic factors, the extracellular matrix, and hormones. However, little is known about the contribution of hormones to peripheral nerve regeneration. Thyroid hormones, which are required for the development and maturation of the central nervous system, are also important for the development of peripheral nerves. The action of triiodothyronine (T3) on responsive cells is mediated through nuclear thyroid hormone receptors (TRs) which modulate the expression of specific genes in target cells. Thus, to study the effect of T3, it is first necessary to know whether the target tissues possess TRs. The fact that sciatic nerve cells possess functional TRs suggests that these cells can respond to T3 and, as a consequence, that thyroid hormone may be involved in peripheral nerve regeneration. The silicone nerve guide model provides an excellent system to study the action of local administration of T3. Evidence from such studies demonstrate that animals treated locally with T3 at the level of transection have more complete regeneration of sciatic nerve and better functional recovery. Among the possible regulatory mechanisms by which T3 enhances peripheral nerve regeneration is rapid action on both axotomized neurons and Schwann cells which, in turn, produce a lasting and stimulatory effect on peripheral nerve regeneration. It is probable that T3 up- or down-regulates gene expression of one or more growth factors, extracellular matrix, or cell adhesion molecules, all of which stimulate peripheral nerve regeneration. This could explain the greater effect of T3 on nerve regeneration compared with the effect of any one growth factor or adhesion molecule.

Animals↗
PubMed2006

[Systemic toxicity caused by local anesthetics after peripheral nerve blocks].

Peripheral nerve blocks have aroused increasing interest in recent years, leading to a rise in the rate of complications. At the same time noteworthy technical advances have been made in areas such as nerve stimulation and ultrasound imaging, and local anesthetics have become safer. Nevertheless, the risk of anesthetic-related systemic toxicity, which manifests with neurological symptoms that tend to be forerunners of cardiovascular ones, can not be ignored. We report 2 cases of systemic toxicity due to the use of a mixture of local anesthetics during nerve blocks for outpatient surgery.

Adult↗